Glutaminolysis and autophagy in cancer

Victor H Villar, Faten Merhi, Mojgan Djavaheri-Mergny, Raúl V Durán

Research output: Contribution to journalReview articlepeer-review


The remarkable metabolic differences between cancer cells and normal cells result in the potential for targeted cancer therapy. The upregulation of glutaminolysis provides energetic advantages to cancer cells. The recently described link between glutaminolysis and autophagy, mediated by MTORC1, may constitute an attractive target for therapeutic strategies. A combination of therapies targeting simultane-ously cell signaling, cancer metabolism, and autophagy can solve therapy resistance and tumor relapse problems, commonly observed in patients treated with most of the current targeted therapies. In this review we summarize the mechanistic link between glutaminolysis and autophagy, and discuss the impacts of these processes on cancer progression and the potential for therapeutic intervention.

Original languageEnglish
Pages (from-to)1198-208
Number of pages11
Issue number8
Publication statusPublished - 2015


  • Animals
  • Autophagy
  • Cell Proliferation
  • Cell Transformation, Neoplastic
  • Drug Resistance, Neoplasm
  • Gene Expression Regulation, Neoplastic
  • Glutamine/metabolism
  • Humans
  • Ketoglutaric Acids/chemistry
  • Mechanistic Target of Rapamycin Complex 1
  • Multiprotein Complexes/metabolism
  • Neoplasm Recurrence, Local
  • Neoplasms/metabolism
  • Reactive Oxygen Species/metabolism
  • Signal Transduction
  • TOR Serine-Threonine Kinases/metabolism


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